Viral Infection
A viral infection begins with a jump into a cellular driver’s seat. To evade detection, that happens very quickly.
Virus try to minimize time in blood or lymph, where they are readily tagged. To do so they take 1 of 2 stratagems.
The 1st is to live awhile in a cell, replicating by hijacking cell machinery. When the virus has met its production quota, it causes the cell to burst open, releasing the next generation of hatchlings to find a new home. This is lysis.
The 2nd technique is for homebodies who take up residence inside a host cell, without killing it. They release offspring from the cell surface without damaging the cell: lysogeny.
Freshly secreted viruses make for a nearby cell to infect. T cells are specialists in detecting viruses hidden within.
Researchers once thought that the AIDS virus was slow on the draw because it took years, even a decade, before symptoms showed. Instead, the long latency is full of furtive activity. The virus is constantly cleared, but, absent a strong immune system or helpful drugs, viral production eventually overwhelms response.
Because T cells are specialized to act against cells bearing pathogens within, T only recognize an antigen derived from these microbes when it appears on the surface of a host cell. T surface receptors, which are similar but not identical to B antibodies, must recognize an antigen plus an alien MHC surface marker that tells the T cell that it is making contact with a foreigner.
Intracellular pathogens only survive inside invaded macrophages by being able to subvert the innate killing mechanisms of these cells. Disabled phages can fight back. An invaded microphage is savvy enough to steal an antigenic fragment from its invader and hoist it to the surface, raising the alarm.
Helper Ts assuredly recognize a virally infected macrophage via a double check. A helper T is first attracted to the ubiquitous class 1 MHC antigens that signal infestation.
The class 2 MHC molecules that phages have are designed to uptake foreign peptides shed by microbes nestled inside pockets within phagocytic cells (vesicles). While the class 2 MHC antigens attracts attention, an infected cell also signals via a surface molecule picked up by another protein on the helper T surface.
This 2-step validation mobilizes T response. Note the neat evolution that macrophages, themselves subject to viral infection, possess such a double-signal system.
Based upon this double check, a helper T produces various cell signaling proteins called cytokines. Cytokines bind to other cells that have matching receptors. That connection influences the behavior and activity of the contacted cell. Some cytokines help B cells make antibodies, while others rouse the hostage macrophage with activating factors that switch on the previously suppressed microbiocidal mechanisms within the phage, thereby killing the invader.
Once a killer T comes into intimate contact with a failing phage it confirms by MHC 1 identification, then delivers the kiss of apoptotic death.
Apoptosis is programmed cell death, commenced by chemical communiqué. A dying cell breaks into smaller pieces, called apobodies (apoptotic bodies), that surrounding cells engulf and digest, preventing what otherwise could be a toxic spill of cell contents.
Veteran lymphocytes become memory cells, thus allowing the body to remember past incursions, and so be better prepared for the next time. Active cell transformation to memory retention is a key mechanism of adaptive immunity.
